Ontology highlight
ABSTRACT:
PROVIDER: PRJNA723409 | ENA |
REPOSITORIES: ENA
Dataset's files
| Action | DRS | |||
|---|---|---|---|---|
| SRR14290429.fastq.gz | Fastqsanger.gz | |||
| SRR14290430.fastq.gz | Fastqsanger.gz | |||
| SRR14290431.fastq.gz | Fastqsanger.gz | |||
| SRR14290432.fastq.gz | Fastqsanger.gz | |||
| SRR14290433.fastq.gz | Fastqsanger.gz |
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Project description:Our previous work identified that type I IFNs mediate macrophage death after infection of Mycobacterium tuberculosis (Mtb) through a novel mechanism.Type I IFN signaling relies on its several hundred ISGs to execute various functions. In order to delineate the downstream mechanism of type I IFN-mediating cell death, we adopted RNA-seq experiments to identify which gene(s) are differentially expressed in WT or Ifnar1-/- bone marrow-derived macrophages (BMDMs). In the meantime, we're also interested in how genetic background affects transcriptomics in BMDMs infected with Mtb. Thus a transcriptomics analysis of C57BL/6, 129S2 and 129X1 infected with Mtb were also conducted.
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Project description:We investigated candidate host-directed therapies for tuberculosis in vitro. BMDMs from tuberculosis susceptible mice B6.Sst1S were stimulated with TNF and infected with Mtb. The infected macrophage were treated with Rocaglamide A, ISRIB and JNK inhibitor SP600125 alone or in combinations to asses the inhibitors' effectas on macrophage transcriptome.
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Project description:Crosstalk between autophagy, host cell death, and inflammatory host responses to bacterial pathogens enables effective innate immune responses that limit bacterial growth while minimizing coincidental host damage. Mycobacterium tuberculosis (Mtb) thwarts innate immune defense mechanisms in alveolar macrophages (AMs) during the initial stages of infection and in recruited bone marrow-derived cells during later stages of infection. However, how protective inflammatory responses are achieved during Mtb infection and the variation of the response in different macrophage subtypes remain obscure. Here, we show that the autophagy receptor Tax1bp1 plays a critical role in enhancing inflammatory cytokine production and increasing the susceptibility of mice to Mtb infection. Surprisingly, although Tax1bp1 restricts Mtb growth during infection of bone marrow-derived macrophages (BMDMs) (Budzik et al. 2020) and terminates cytokine production in response to cytokine stimulation or viral infection, Tax1bp1 instead promotes Mtb growth in AMs, neutrophils, and a subset of recruited monocyte-derived cells from the bone marrow. Tax1bp1 also leads to increases in bacterial growth and inflammatory responses during infection of mice with Listeria monocytogenes, an intracellular pathogen that is not effectively targeted to canonical autophagy. In Mtb-infected AMs but not BMDMs, Tax1bp1 enhances necrotic-like cell death early after infection, reprogramming the mode of host cell death to favor Mtb replication in AMs. Tax1bp1’s impact on host cell death is a mechanism that explains Tax1bp1’s cell type-specific role in the control of Mtb growth. Similar to Tax1bp1-deficiency in AMs, the expression of phosphosite-deficient Tax1bp1 restricts Mtb growth. Together, these results show that Tax1bp1 plays a crucial role in linking the regulation of autophagy, cell death, and pro-inflammatory host responses and enhancing susceptibility to bacterial infection.
2025-10-15 | PXD064244 | Pride
Project description:Mtb appears to have developed specialized biomolecular infrastructure to survive and persist within granulomas, where it is subjected to a diverse set of stress conditions. One of these stress conditions is hypoxia. We hypothesized that host cell response is radically altered with hypoxia stressed Mtb and designed in-vitro experiments to study this phenomenon. Hypoxia-stressed as well as aerobically grown Mtb were used to infect rhesus macaque bone marrow derived macrophages (Rh-BMDMs) and the host global transcriptional response compared. Using 4 x44 k Agilent arrays specific for rhesus macaque genome, we tested in biological duplicate the effect of aerogically grown Mtb on rhesus macaque BMDMs and compared this to the corresponding effect of the hypoxia-conditioned Mtb on rhesus macaque BMDMs
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Project description:Purpose: The goal of this study was the transcriptome high-throughput data analysis of spleen cells from mice infected with a virulent strain of mycobacterium (H37rv) and either fed ad libitum (AL) or caloric restricted (CR) Methods: Spleen cell total RNA profile of 17 weeks old mice (1. MTB infected, Ad libitum fed; 2. MTB infected, Caloric restricted; 3. Not infected, Ad libitum fed; 4. Not infected, Caloric restricted; a pool of 5 animals per group) were generated by deep sequencing, in triplicate, using TruSeq Stranded Total RNA Illumina technology Results: Principal component analysis and unsupervised clustering showed that the RNA-seq profiles of spleen cells from these four groups of mice were clearly distinct and infection was the major force affecting gene expression, with 67% of variance coming from the infection status and another 23% variance being dependent on caloric intake . When directly comparing AL versus CR MTB infected spleens, 628 genes were found differentially expressed. Supervised hierarchical clustering based on the expression of these 628 genes was able to unveil the unique transcriptional profile of CR MTB infected mice compared to both AL MTB infected and Not infected mice. Coclusions: Caloric restriction is able to affect the expression of a significant number of genes in spleen cells isolated from mice infected with MTB. The study of biological process enrichements highlights relevant immune-related regulation in these animals, than may be at the base of the higher capacity of caloric restricted, compared to ad libitum fed, animals to resist MTB infection.
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Project description:The BCG vaccine has been used against tuberculosis (TB) for over hundred years; however, it does not protect adults from pulmonary TB. To develop alternative vaccines against TB, we generated Mycobacterium tuberculosis H37Rv (Mtb)-derived vaccine strains by rationally deleting key virulent genes, resulting in single (SKO; ΔfbpA), double (DKO; ΔfbpA-ΔsapM), triple (TKO-D; ΔfbpA-ΔsapM-ΔdosR and TKO-Z; ΔfbpA-ΔsapM-Δzmp1), and quadruple (QKO; ΔfbpA-ΔsapM-Δzmp1-dosR) strains. To understand how macrophages, the host cells that defend against infection and process antigens for presentation to immune cells, respond to these vaccine strains, we performed transcriptomic analyses of mouse bone marrow-derived macrophages (BMDMs) infected with these strains. The transcriptomic data were compared with similar data obtained from macrophages infected with Mtb H37Rv and BCG. Our analyses revealed that genes associated with various immune and cell signaling pathways, such as NF-kappa B signaling, TNF signaling, cytokine-cytokine receptor interaction, chemokine signaling, hematopoietic cell lineage, Toll-like receptor signaling, IL-17 signaling, Th1 and Th2 cell differentiation, Th17 cell differentiation, and T cell receptor signaling were differentially expressed in BMDMs infected with our vaccine strains. Enhanced expression of cytokines and chemokines, including proinflammatory cytokines such as TNF-α, IL-6, GM-CSF, and IL-1, which are essential for the immune response against Mtb infection, was also observed in BMDMs infected with these strains. In particular, BMDMs infected with all vaccine strains exhibited a significant upregulation of genes associated with the IL-17 pathway. These results may indicate that our vaccine strains could induce a protective immune response against TB.
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Project description:Crosstalk between autophagy, host cell death, and inflammatory host responses to bacterial pathogens enables effective innate immune responses that limit bacterial growth while reducing coincidental host damage. Mycobacterium tuberculosis thwarts innate immune defense mechanisms in alveolar macrophages (AMs) during the initial stages of infection and in recruited bone marrow-derived cells during later stages of infection. How protective inflammatory responses are achieved during Mycobacterium tuberculosis (Mtb) infection and the differences in these responses in macrophage subtypes are obscure. Here, we discovered that the autophagy receptor Tax1bp1 plays a critical role in enhancing inflammatory cytokine production and promoting the susceptibility of mice to infection with Mtb. These results were surprising because Tax1bp1 instead restricts Mtb growth during infection of bone marrow-derived macrophages (BMDMs), as we previously showed (Budzik et al. 2020), and terminates cytokine production in response to cytokine stimulation or viral infection. Tax1bp1 also leads to increases in bacterial growth and inflammatory responses during infection of mice with Listeria monocytogenes, an intracellular pathogen that is not effectively targeted to canonical autophagy. In contrast to its role in restricting Mtb growth in BMDMs, Tax1bp1 promotes Mtb growth in AMs, neutrophils, and recruited monocyte-derived cells from the bone marrow. In Mtb-infected AMs, Tax1bp1 enhances necrosis and inflammatory cytokine synthesis while restraining apoptosis, changing the mode of host cell death to favor Mtb replication. Similar to Tax1bp1-deficiency in AMs, the expression of phosphosite-deficient Tax1bp1 restricts Mtb growth. Together, these results show that Tax1bp1 plays a crucial role in linking the regulation of autophagy, cell death, and pro-inflammatory host responses to augment susceptibility to bacterial infection.
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Project description:The purpose of this study was to identify Mtb- and hsa-encoded miRNAs produced in infected macrophages. RNA from 9 THP-1 samples (3 were uninfected, 3 were infected with Mtb H37Rv for 3 days and 3 were infected with Mtb H37Rv for 6 days) was sequenced and miRNAs were detected.
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Project description:Next-generation sequencing (NGS) has revolutionized systems-based analysis of cellular pathways. The goals of this study is to compare gene expression (RNA-seq) profile between Mtb infected Fth+/+ and Fth-/- mice at 9 weeks post Mtb infection. Gene expression analysis demonstrated an essential role for FtH in mitochondrial function and maintenance of central intermediary metabolism in vivo
2018-09-01 | GSE112361 | GEO